Endocarditis

Endocarditis

EndocarditisClassifications and external resources

Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis. The bacilli appear as black granulations.

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Endocarditis can be classified by etiology as either infective or non-infective, depending on whether a microorganism is the source of the problem.
Contents

1 Infective endocarditis
1.1 Classification
1.2 Etiology and pathogenesis
1.3 Clinical and pathological features
1.4 Diagnosis
1.5 Micro-organisms responsible
1.6 Treatment
2 Non-infective endocarditis
3 References
4 External links
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] Infective endocarditis
As the valves of the heart do not actually receive any blood supply of their own, which may be surprising given their location, defense mechanisms (such as white blood cells) cannot enter. So if an organism (such as bacteria) establish hold on the valves, the body cannot get rid of them.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) bacteria have a chance to take hold.
Classification
Traditionally, infective endocarditis has been clinically divided into acute and subacute (between acute and chronic) endocarditis. This classifies both the tempo of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred despite the lack of advantage in meaning.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be fastidious because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important.
The Russian classification includes "endocarditis in narcotic abusers" in addition to above given classification, as this disease is very common in narcotic drug users who inject with non-sterile injections/syringes.
Etiology and pathogenesis
As previously mentioned, altered blood flow around the valves is a risk factor in obtaining endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).
In a healthy individual, a bacteraemia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with a piece of a blood clot, the valve provides a place for the bacteria to attach themselves and an infection can be established.
The bacteraemia is often caused by minor dental procedures, such as a tooth removal. It is important that a dentist is told of any heart problems before commencing.
Another group of causes result from a high number of bacteria getting into the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of bacteria. With a large number of bacteria, even a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus) is usually responsible for infecting a normal valve.
Intravenous drug users tend to get their right heart valves infected because the veins that are injected enter the right side of the heart. The injured valve is most commonly affected when there is a pre-existing disease. (In rheumatic heart disease this is the aortic and the mitral valves, on the left side of the heart.)
Clinical and pathological features
Fever (often spiking)
Continuous presence of micro-organisms in the bloodstream determined by serial collection of blood cultures
Vegetations on valves on echocardiography
Septic emboli, causing circulatory problems (stroke, gangrene of fingers)
Chronic renal failure
Osler's nodes (painful subcutaneous lesions in the distal fingers)
Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
Roth spots on the retina
Conjunctival petechiae
A new or changing heart murmur, particularly murmurs suggestive of valvular incompetence
Splinter hemorrhages
Diagnosis
In general, a patient should fulfill the Duke Criteria[1] in order to establish the diagnosis of endocarditis.
As the Duke Criteria relies heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse[2][3][4] and among non drug abusing patients [5][6]. Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococcus make the following estimates incorrectly low.
Among patients who do not use illicit drugs and have a fever in the emergency room, there is a less than 5% chance of occult endocarditis. Mellors [6] in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patients in the emergency room. The upper confidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici [5] found that among 113 non-selected adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.
Among patients who do use illicit drugs and have a fever in the emergency room, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever[4]. Weisse[2] found that 13% of 121 patients had endocarditis. Marantz [4] also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. Samet [3] found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.
Among patients with staphylococcal bacteremia (SAB), one study found a prevalence of 29% in community-acquired SAB versus 5% in nosocomial SAB[7]. However, only 2% of strains were resistant to methicillen and so these numbers may be low in areas of higher resistance.
EchocardiographyThe transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis[8][9].
[Discussion is needed here, including transthoracic versus transesophageal]
Micro-organisms responsible
Many types of organism can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is removed, and any growth is noted and identified.
Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is common.
A third important cause of endocarditis is Enterococci. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococci are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired endocarditis.
Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
Candida albicans, a yeast, is associated with IV drug users and the immunocompromised.
Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water.
Streptococcus bovis, which is part of the natural flora of the bowel, tends to present when the patient has bowel cancer.
HACEK organisms are a group of bacteria that live on the dental gums, and are associated with IV drug users who contaminate their needles with saliva.
Treatment
High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves. Infective endocarditis is associated with a 25% mortality.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancers, particularly mucinous adenocarcinoma.
References
^ Durack D, Lukes A, Bright D (1994). "New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service.". Am J Med 96 (3): 200-9. PMID 8154507.
^ a b Weisse A, Heller D, Schimenti R, Montgomery R, Kapila R (1993). "The febrile parenteral drug user: a prospective study in 121 patients.". Am J Med 94 (3): 274-80. PMID 8452151.
^ a b Samet J, Shevitz A, Fowle J, Singer D (1990). "Hospitalization decision in febrile intravenous drug users.". Am J Med 89 (1): 53-7. PMID 2368794.
^ a b c Marantz P, Linzer M, Feiner C, Feinstein S, Kozin A, Friedland G (1987). "Inability to predict diagnosis in febrile intravenous drug abusers.". Ann Intern Med 106 (6): 823-8. PMID 3579068.
^ a b Leibovici L, Cohen O, Wysenbeek A (1990). "Occult bacterial infection in adults with unexplained fever. Validation of a diagnostic index.". Arch Intern Med 150 (6): 1270-2. PMID 2353860.
^ a b Mellors J, Horwitz R, Harvey M, Horwitz S (1987). "A simple index to identify occult bacterial infection in adults with acute unexplained fever.". Arch Intern Med 147 (4): 666-71. PMID 3827454.
^ Kaech C, Elzi L, Sendi P, Frei R, Laifer G, Bassetti S, Fluckiger U (2006). "Course and outcome of Staphylococcus aureus bacteraemia: a retrospective analysis of 308 episodes in a Swiss tertiary-care centre.". Clin Microbiol Infect 12 (4): 345-52. PMID 16524411.
^ Shively B, Gurule F, Roldan C, Leggett J, Schiller N (1991). "Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis.". J Am Coll Cardiol 18 (2): 391-7. PMID 1856406. ^ Erbel R, Rohmann S, Drexler M, Mohr-Kahaly S, Gerharz C, Iversen S, Oelert H, Meyer J (1988). "Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study.". Eur Heart J 9 (1): 43-53. PMID 3345769